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Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to Excessive Angiogenesis
M2 macrophage (Mφ) promotes pathologic angiogenesis through a release of pro-angiogenic mediators or the direct cell–cell interaction with endothelium in the micromilieu of several chronic inflammatory diseases, including rheumatoid arthritis and cancer, where interleukin (IL)-18 also contributes to...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5845536/ https://www.ncbi.nlm.nih.gov/pubmed/29559970 http://dx.doi.org/10.3389/fimmu.2018.00334 |
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author | Kobori, Takuro Hamasaki, Shinichi Kitaura, Atsuhiro Yamazaki, Yui Nishinaka, Takashi Niwa, Atsuko Nakao, Shinichi Wake, Hidenori Mori, Shuji Yoshino, Tadashi Nishibori, Masahiro Takahashi, Hideo |
author_facet | Kobori, Takuro Hamasaki, Shinichi Kitaura, Atsuhiro Yamazaki, Yui Nishinaka, Takashi Niwa, Atsuko Nakao, Shinichi Wake, Hidenori Mori, Shuji Yoshino, Tadashi Nishibori, Masahiro Takahashi, Hideo |
author_sort | Kobori, Takuro |
collection | PubMed |
description | M2 macrophage (Mφ) promotes pathologic angiogenesis through a release of pro-angiogenic mediators or the direct cell–cell interaction with endothelium in the micromilieu of several chronic inflammatory diseases, including rheumatoid arthritis and cancer, where interleukin (IL)-18 also contributes to excessive angiogenesis. However, the detailed mechanism remains unclear. The aim of this study is to investigate the mechanism by which M2 Mφs in the micromilieu containing IL-18 induce excessive angiogenesis in the in vitro experimental model using mouse Mφ-like cell line, RAW264.7 cells, and mouse endothelial cell line, b.End5 cells. We discovered that IL-18 acts synergistically with IL-10 to amplify the production of Mφ-derived mediators like osteopontin (OPN) and thrombin, yielding thrombin-cleaved form of OPN generation, which acts through integrins α4/α9, thereby augmenting M2 polarization of Mφ with characteristics of increasing surface CD163 expression in association with morphological alteration. Furthermore, the results of visualizing temporal behavior and morphological alteration of Mφs during angiogenesis demonstrated that M2-like Mφs induced excessive angiogenesis through the direct cell–cell interaction with endothelial cells, possibly mediated by CD163. |
format | Online Article Text |
id | pubmed-5845536 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-58455362018-03-20 Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to Excessive Angiogenesis Kobori, Takuro Hamasaki, Shinichi Kitaura, Atsuhiro Yamazaki, Yui Nishinaka, Takashi Niwa, Atsuko Nakao, Shinichi Wake, Hidenori Mori, Shuji Yoshino, Tadashi Nishibori, Masahiro Takahashi, Hideo Front Immunol Immunology M2 macrophage (Mφ) promotes pathologic angiogenesis through a release of pro-angiogenic mediators or the direct cell–cell interaction with endothelium in the micromilieu of several chronic inflammatory diseases, including rheumatoid arthritis and cancer, where interleukin (IL)-18 also contributes to excessive angiogenesis. However, the detailed mechanism remains unclear. The aim of this study is to investigate the mechanism by which M2 Mφs in the micromilieu containing IL-18 induce excessive angiogenesis in the in vitro experimental model using mouse Mφ-like cell line, RAW264.7 cells, and mouse endothelial cell line, b.End5 cells. We discovered that IL-18 acts synergistically with IL-10 to amplify the production of Mφ-derived mediators like osteopontin (OPN) and thrombin, yielding thrombin-cleaved form of OPN generation, which acts through integrins α4/α9, thereby augmenting M2 polarization of Mφ with characteristics of increasing surface CD163 expression in association with morphological alteration. Furthermore, the results of visualizing temporal behavior and morphological alteration of Mφs during angiogenesis demonstrated that M2-like Mφs induced excessive angiogenesis through the direct cell–cell interaction with endothelial cells, possibly mediated by CD163. Frontiers Media S.A. 2018-03-06 /pmc/articles/PMC5845536/ /pubmed/29559970 http://dx.doi.org/10.3389/fimmu.2018.00334 Text en Copyright © 2018 Kobori, Hamasaki, Kitaura, Yamazaki, Nishinaka, Niwa, Nakao, Wake, Mori, Yoshino, Nishibori and Takahashi. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Kobori, Takuro Hamasaki, Shinichi Kitaura, Atsuhiro Yamazaki, Yui Nishinaka, Takashi Niwa, Atsuko Nakao, Shinichi Wake, Hidenori Mori, Shuji Yoshino, Tadashi Nishibori, Masahiro Takahashi, Hideo Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to Excessive Angiogenesis |
title | Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to Excessive Angiogenesis |
title_full | Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to Excessive Angiogenesis |
title_fullStr | Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to Excessive Angiogenesis |
title_full_unstemmed | Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to Excessive Angiogenesis |
title_short | Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to Excessive Angiogenesis |
title_sort | interleukin-18 amplifies macrophage polarization and morphological alteration, leading to excessive angiogenesis |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5845536/ https://www.ncbi.nlm.nih.gov/pubmed/29559970 http://dx.doi.org/10.3389/fimmu.2018.00334 |
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